Atlante A, Seccia T M, Pierro P, Vulpis V, Marra E, Pirrelli A, Passarella S
Centro di Studio sui Mitocondri e Metabolismo Energetico, CNR, Bari, Italy.
Int J Mol Med. 1998 Apr;1(4):709-16. doi: 10.3892/ijmm.1.4.709.
Use was made of mitochondria isolated from heart left ventricles of either spontaneously hypertensive or age-matched Wistar-Kyoto rats used as a control to find out whether hypertrophy (5-week-old rats) or hypertrophy/hypertension (24-week-old rats) can cause change in the mechanisms by which ATP is synthesised via ATP synthase and subsequently exported via the ADP/ATP translocator outside mitochondria. To do this, photometric measurements were made of the rate of ATP appearance in the extramitochondrial phase, which occurs as a result of ADP addition to mitochondria. In mitochondria from spontaneously hypertensive rats deficit of ATP production was found dependent on changes in the KmADP and Vmax values of both the ADP/ATP translocator and the ATP synthase. The ADP/ATP translocator was found to determine the rate of ATP production outside mitochondria in all the tested samples. In an initial investigation carried out to ascertain how cell ATP deficit can be counterbalanced, an increase in both adenylate kinase and creatine kinase activities was found in both hypertrophy and hypertrophy/hypertension. A possible increase in anaerobic glycolysis was also suggested by the increased lactate dehydrogenase activity.
利用从自发性高血压大鼠或作为对照的年龄匹配的Wistar-Kyoto大鼠的心脏左心室分离的线粒体，以探究肥大（5周龄大鼠）或肥大/高血压（24周龄大鼠）是否会导致通过ATP合酶合成ATP并随后通过ADP/ATP转位酶输出到线粒体外的机制发生变化。为此，对向线粒体中添加ADP后线粒体外相中ATP出现的速率进行了光度测量。在自发性高血压大鼠的线粒体中，发现ATP产生不足取决于ADP/ATP转位酶和ATP合酶的KmADP和Vmax值的变化。在所有测试样品中，发现ADP/ATP转位酶决定线粒体外ATP的产生速率。在最初进行的确定细胞ATP不足如何得到平衡的研究中，发现在肥大和肥大/高血压状态下，腺苷酸激酶和肌酸激酶的活性均增加。乳酸脱氢酶活性增加也提示无氧糖酵解可能增加。
